*Received for publication October 28, 1957.From the Department of Medicine, The Johns Hopkins University School of Medicine and Hospital.†Department of Medicine of the Howard Hughes Medical Institute.This investigation was supported in part by a Research Grant of the Division of Research Grants and Fellowships, National Institutes of Health.Requests for reprints should be addressed to Ernest W. Smith, M.D., Assistant Professor of Medicine, The Johns Hopkins Hospital, Baltimore 5, Maryland.

Abstract

Soon after the discovery that sickle (S) hemoglobin can be differentiated from normal (A) hemoglobin by electrophoresis,1 other abnormalities of hemoglobin were recognized. In studying a white patient who previously had been thought to have sickle cell anemia, Itano2 found that the erythrocytes of the mother could not be made to sickle, although the electrophoretic pattern was indistinguishable from that of sickle cell trait. The abnormal hemoglobin which did not produce sickling also differed from S hemoglobin because of its normal solubility in the reduced state, and was subsequently designated as hemoglobin D. The atypical hemolytic disorder in the patient